Nonrandom chromosome abnormalities have been identified in human myelogenous leukemia, both chronic and acute. In addition to the translocation usually involving chromosomes no. 9 and 22 in chronic myleoid leukemia, we have identified three structural rearrangements that recur in patients with acute myeloid leukemia. Two of these were described in previous years, namely, a translocation involving chromosomes no. 8 and 21 in acute myeloblastic leukemia with maturation and one involving chromosomes no. 15 and 17 in acute promyelocytic leukemia (APL). We have identified this translocation in all 27 patients with APL whom we have studied. This past year, we have identified a new aberration, namely, a pericentric inversion of no. 16 in acute myelomonocytic leukemia (AMMoL). This abnormality is found in about 25% of our patients with AMMoL. We have increased our series of patients who have leukemia following cytotoxic treatment of either a malignant (lymphoma, multiple myeloma or cancer) or nonmalignant (renal transplant) disease. We have analyzed the karyotypes of more than 60 patients and find an abnormal pattern in more than 90%. Two abnormalities occur in greater than 80% of the patients. These include the loss of all or the long arm of no. 5 and/or no. 7. Detailed analysis of the portion of no. 5 that is consistently missing from all cells reveals that 5q31 is deleted in all cases; similar analysis for no. 7 shows that the consistent deletion involves the area q34 to near the terminal region. The recent explosion of scientific information regarding oncogenes and cancer has been remarkable because of the close correlation between the chromosome location of oncogenes with the chromosome abnormalities, especially translocations that we have identified in human leukemia and lymphoma. The use of sophisticated DNA technology will provide us with substantial insights into the nature of the genes at the breakpoints of these consistent abnormalities. It will be possible to determine whether some of the breakpoints involve oncogenes and if so how the break in the DNA of these special genes is related to the malignant change. This in turn should lead to more effective therapy in the future.